Measurement and implications of the Q˙s/Q˙t

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Measurement and implications of the s/t

Robert A. Strickland, MD

Hypoxemia can be caused by a variety of factors (Box 32-1). This chapter will focus on the primary cause of hypoxemia—shunting, which may, at times, be due to ventilation/perfusion (/) mismatch.

Box 32-1 Causes of Hypoxemia

An O₂-deficient environment, such as occurs at high altitude

Hypoventilation, which can be caused by the use of opioid or sedative agents

Diffusion abnormalities at the alveolar-capillary membrane

Ventilation/perfusion mismatch

Ideally, pulmonary perfusion () evenly matches alveolar ventilation at all levels of the lung; however, perfect matching does not occur because the distribution of ventilation and perfusion and the / ratio vary throughout the lung. A normal lung has a / ratio of approximately 0.8. A / ratio of 0 (i.e., a shunt) exists when perfused alveoli have no ventilation and the values for PO₂ and PCO₂ of the trapped air are the same as those of mixed venous blood (PO₂ = 40 mm Hg and PCO₂ = 47 mm Hg). Conversely, a / ratio of ∞ exists when ventilated alveoli have no perfusion and, at sea level, the PO₂ and PCO₂ equal approximately 150 and 0 mm Hg, respectively. Nonperfused alveoli (i.e., alveolar dead space) is approximately 25 to 50 mL in a healthy 70-kg person. Figure 32-1 depicts the progression of a / ratio from 0 to ∞; the normal, idealized, alveolar-capillary unit is shown as example A.

Figure 32-1 Effect of altering the ventilation-perfusion ratio on the PO₂ and PCO₂ in a lung unit from 0 (B) to normal (A) to ∞ (C). (From West JB. Respiratory physiology: the essentials. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2012:64.)

In contrast with blood vessels in all other tissues, which dilate in response to hypoxemia, the blood vessels of intact lung constrict in response to hypoxia (termed hypoxic pulmonary vasoconstriction [HPV]). Blood flow is directed away from poorly ventilated regions of a lung to better ventilated lung fields. Thus, the overall / ratio improves, better oxygenating blood. A low PO₂ in the pulmonary arteries and pulmonary capillaries is the predominant stimulus that produces HPV, although a low mixed venous O₂ pressure (PO₂) also plays a role. A PO₂ below 100 mm Hg will initiate HPV; marked vasoconstriction occurs with a PO₂ less than 70 mm Hg, becoming progressively more severe as PO₂ levels continue to decrease. The mechanism for HPV is not well understood, but it appears that pulmonary vascular endothelium responds to a low O₂ tension, with endothelium-derived vasoconstrictor biochemicals (e.g., leukotrienes and prostaglandins) constricting arteriolar smooth muscle.

A variety of physiologic alterations and pharmacologic interventions alter HPV. Respiratory acidosis and metabolic acidosis increase HPV, whereas respiratory alkalosis and metabolic alkalosis decrease HPV. In vitro studies have shown that inhaled anesthetic agents uniformly inhibit HPV, but the results of in vivo studies have not often yielded clinically significant effects. Systemically administered vasodilators, such as nitroprusside and nitroglycerin, generally adversely affect HPV, which may be of consequence in patients with significant obstructive lung disease or during one-lung ventilation.

Shunting due to other causes

A small fraction of blood in the cardiac output, normally 2% to 5%, enters the arterial circulation without first passing through the pulmonary circulation, accounting for the normal O₂ alveolar-arterial gradient P(A-a)O₂. The causes for this type of venous admixture include (1) the thebesian veins, which drain blood from the coronary circulation directly into the left atrium and, rarely, the left ventricle and (2) the bronchial vein, which provides the nutritive perfusion of the bronchial tree and pleura. Abnormal anatomic shunts include right-to-left atrial and ventricular septal defects and pulmonary arteriovenous malformations.

Hypoxemia that is the result of a physiologic or anatomic shunt cannot be corrected by having the patient breathe supplemental O₂. The hemoglobin in blood that perfuses alveoli with a / ratio of 1 will readily achieve 100% saturation; increasing the partial pressure of O₂ in these alveoli will minimally increase the O₂ content. Blood that perfuses alveoli with a / ratio of 0 will not be exposed to any O₂, no matter the fraction of inspired O₂ (FIO₂); therefore, no significant improvement in arterial oxygenation occurs (Figure 32-2).

Figure 32-2 Ventilation-perfusion relationships. In the standing position, the effects of gravity result in gradients in both perfusion and ventilation of the lung from base to apex. Because the perfusion gradient is steeper than the ventilation gradient, the ratio of ventilation to perfusion (A/c), is lowest at the bottom of the lung and greatest at the top of the lung (B). A/c is also affected by various other conditions affecting ventilation and perfusion (A and B). (Netter illustration from www.netterimages.com. © Elsevier Inc. All rights reserved.)

Figure 32-2 Ventilation-perfusion relationships. In the standing position, the effects of gravity result in gradients in both perfusion and ventilation of the lung from base to apex. Because the perfusion gradient is steeper than the ventilation gradient, the ratio of ventilation to perfusion (A/c), is lowest at the bottom of the lung and greatest at the top of the lung (B). A/c is also affected by various other conditions affecting ventilation and perfusion (A and B). (Netter illustration from www.netterimages.com. © Elsevier Inc. All rights reserved.)

As previously stated, the normal shunt fraction is less than 5%. Clinically significant shunts equal 10% to 20% of cardiac output, whereas potentially fatal shunts are usually greater than 30%. Seldom does a shunt result in an elevated PaCO₂. Chemoreceptors sense elevations in PaCO₂ and increase ventilation. The PaCO₂ of unshunted blood is reduced, and the overall PaCO₂ is usually normal. If ventilatory drive related to a low PaO₂ produces significant hyperventilation, it is possible to actually have a PaCO₂ that is less than normal.

Calculation of shunt fraction

The fraction of cardiac output that passes through the various shunts is expressed as the shunt fraction (s/t):

< ?xml:namespace prefix = "mml" />Q˙s/Q˙t = (CcO2–CaO2)/(CcO2–CvO2)

where Cc equals the O₂ content of end-pulmonary capillary blood, Ca is the O₂ content of arterial blood, and C represents the O₂ content of mixed venous blood. The O₂ content of arterial blood is calculated by:

Ca = 1.39(hemoglobin concentration) (% O2saturation) + 0.003(PaO2)

The O₂ contents of Cc and of C are calculated by inserting the respective O₂ saturation and PaO₂ values into the equations.

When cardiac output and hemoglobin concentration are normal and the PaO₂ is greater than 175 mm Hg, the shunt fraction can be estimated by using the simplified formula:

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